The Journal of Thoracic and Cardiovascular Surgery
Volume 139, Issue 6 , Pages 1676-1677, June 2010

Reply to the Editor

Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pa

Article Outline

CTSNet classification: 23, 29, 38.2

 

With great interest, we read Picichè and associates' letter entitled, “Angiogenesis and surgical or endovascular enhancement of noncoronary collateral circulation: a new research field.” We thank the authors for their kind comments regarding our article on the neovasculogenic effects of transmyocardial revascularization. We agree wholeheartedly with the authors that in patients with coronary artery disease, noncoronary collateral circulation and the microvasculature comprise critical components of myocardial perfusion and viability and hence greatly affect cardiomyocyte and ventricular function. Although surgical and percutaneous coronary therapy and investigative research are focused predominantly on large epicardial coronary vessels, the small collaterals and microvasculature are greatly underappreciated and understudied.

Certainly there are abundant clinical anecdotes of patients surviving on various permutations of coronary and noncoronary collaterals. Clinicians have all encountered the patient with an angiographically absent major coronary artery yet with the subtended myocardium demonstrating completely normal contractility on echocardiographic analysis. Is such a large region supplied through coronary collaterals, noncoronary collaterals from the base of the heart and posterior pericardial reflection or perhaps through the highly vascularized adhesions that surgeons encounter when operating on patients with prior cardiac surgery, renal failure, or myocardial infarction and Dressler syndrome? In older patients and in states of chronic disease, the ability to generate such collaterals can be impaired.1, 2 Researchers are beginning to understand the critical interrelated roles of endogenous myocardium-mediated proangiogenic signaling and bone marrow–derived endothelial progenitor cells.3, 4 Although initially very promising, the results of clinical trials aimed at harnessing this intrinsic revascularization machinery have been clinically equivocal.5, 6, 7 Perhaps what is needed is a refocus on augmenting noncoronary collaterals as an additional driving force in therapeutic neovascularization.

The authors present a very intriguing strategy of ligating both distal internal thoracic arteries to produce a regional state of hypertension and hyperperfusion around the mediastinum. Coupled with local delivery of angiogenic cytokines, the authors propose to enhance the development of noncoronary collaterals to reperfuse the ischemic myocardium in 2 large animal models. The preliminary background data presented by the authors is encouraging. Although critics will focus on the preclusion of a future left internal thoracic artery–left anterior descending coronary artery graft, the cornerstone of coronary artery bypass grafting surgery, the experimental hypothesis is conceptually exciting and should be carefully investigated. The authors' proposal is uniquely novel and highly innovative, and we certainly look forward to the findings with great anticipation.

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References 

  1. Sodha NR, Clements RT, Boodhwani M, Xu SH, Laham RJ, Bianchi C, et al. Endostatin and angiostatin are increased in diabetic patients with coronary artery disease and associated with impaired coronary collateral formation. Am J Physiol Heart Circ Physiol. 2009;296:H428–H434
  2. Zhuo Y, Li SH, Chen MS, Wu J, McDonald Kinkaid HY, Fazel S, et al. Aging impairs the angiogenic response to ischemic injury and the activity of implanted cells: combined consequences for cell therapy in older recipients. J Thorac Cardiovasc Surg. 2009;[Epub ahead of print]
  3. Kwon SM, Eguchi M, Wada M, Iwami Y, Hozumi K, Iwaguro H, et al. Specific Jagged-1 signal from bone marrow microenvironment is required for endothelial progenitor cell development for neovascularization. Circulation. 2008;118:157–165
  4. Kawamoto A, Iwasaki H, Kusano K, Murayama T, Oyamada A, Silver M, et al. CD34-positive cells exhibit increased potency and safety for therapeutic neovascularization after myocardial infarction compared with total mononuclear cells. Circulation. 2006;114:2163–2169
  5. Assmus B, Honold J, Schachinger V, Britten MB, Fischer-Rasokat U, Lehmann R, et al. Transcoronary transplantation of progenitor cells after myocardial infarction. N Engl J Med. 2006;355:1222–1232
  6. Schachinger V, Erbs S, Elsasser A, Haberbosch W, Hambrecht R, Holschermann H, et al. Intracoronary bone marrow-derived progenitor cells in acute myocardial infarction. N Engl J Med. 2006;355:1210–1221
  7. Wollert KC, Meyer GP, Lotz J, Ringes-Lichtenberg S, Lippolt P, Breidenbach C, et al. Intracoronary autologous bone-marrow cell transfer after myocardial infarction: the BOOST randomised controlled clinical trial. Lancet. 2004;364:141–148

PII: S0022-5223(10)00264-3

doi:10.1016/j.jtcvs.2010.03.005

Refers to article:

  • Angiogenesis and surgical or endovascular enhancement of noncoronary collateral circulation: A new research field

    Marco Picichè, John G. Kingma, Pierre Voisine, Francois Dagenais, Elie Fadel
    The Journal of Thoracic and Cardiovascular Surgery June 2010 (Vol. 139, Issue 6, Pages 1675-1676)

The Journal of Thoracic and Cardiovascular Surgery
Volume 139, Issue 6 , Pages 1676-1677, June 2010

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